ch 17 Flashcards
What happens at the synaptic terminal during neurotransmitter release?
When an action potential reaches the axon terminal, voltage-gated Ca2+ channels open, allowing calcium to enter.
This triggers vesicle fusion and the release of neurotransmitters into the synaptic cleft via exocytosis.
Describe the role of the sodium-potassium pump in resting membrane potential.
The pump maintains resting membrane potential by using ATP to move 3 Na+ ions out of the cell and 2 K+ ions into the cell, creating a negative charge inside the cell.
Explain the difference between graded potentials and action potentials
Graded potentials are local, variable, and dependent on stimulus strength.
action potentials are “all-or-none” and propagate without loss of signal strength.
How does saltatory conduction increase action potential speed?
In myelinated axons, the action potential “jumps” between nodes of Ranvier, where voltage-gated channels are concentrated. This increases signal speed by reducing the need for regeneration along the entire axon.
What is the role of calcium ions at the presynaptic terminal?
Calcium ions trigger the fusion of neurotransmitter vesicles with the presynaptic membrane, facilitating neurotransmitter release into the synaptic cleft.
Describe the phases of an action potential.
Depolarization: Voltage-gated Na+ channels open, and Na+ enters the cell.
Repolarization: K+ channels open, allowing K+ to leave the cell.
Hyperpolarization: K+ channels remain open briefly, overshooting resting potential.
How do G-protein-coupled receptors differ from ionotropic receptors?
Ionotropic receptors directly open ion channels when a neurotransmitter binds.
Metabotropic receptors activate G-proteins, which indirectly influence channels or other cellular processes via second messengers.
Describe the process of neurotransmitter removal from the synaptic cleft and explain why it is essential for neural signaling.
Neurotransmitter removal from the synaptic cleft is crucial to terminate the signal and prevent continuous activation of the postsynaptic neuron. This removal occurs in three main ways:
Diffusion: Neurotransmitters diffuse away from the synaptic cleft.
Enzymatic breakdown: Enzymes (e.g., acetylcholinesterase) break down neurotransmitters.
Reuptake: Neurotransmitters are actively transported back into the presynaptic neuron or nearby glial cells for recycling.
How do myelinated axons increase the speed of action potential propagation compared to unmyelinated axons?
In myelinated axons, the action potential propagates through saltatory conduction, where the depolarization “jumps” between the nodes of Ranvier (gaps in the myelin sheath). Myelin acts as an insulator, preventing ion leakage and allowing the depolarization to travel quickly through the myelinated segments. Action potentials are only regenerated at the nodes, where voltage-gated Na+ channels are concentrated, dramatically increasing the conduction speed.
In contrast, unmyelinated axons rely on continuous conduction, where action potentials must be regenerated at every segment of the membrane, making the process slower.
